Coherently, studies both in MS and in the EAE mouse model, revealed that pro-inflammatory cytokines, such as Interleukin-1β (IL-1β) and Tumor Necrosis Factor (TNF), released from infiltrating T cells and from activated microglia and astroglia, participate in the early imbalance between glutamate excitatory and GABA inhibitory transmission, leading to hyperexcitability and excitotoxic neuronal damage in several brain areas [7, 8]. The gene discussed is IL1B; the disease is myeloid sarcoma.